Tumor regression and resistance mechanisms upon CDK4 and RAF1 inactivation in KRAS/P53 mutant lung adenocarcinomas.

doi:10.1073/pnas.2002520117

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Article

Tumor regression and resistance mechanisms upon CDK4 and RAF1 inactivation in KRAS/P53 mutant lung adenocarcinomas.

Proceedings of the National Academy of Sciences of the United States of America - 29 Sept 2020

Esteban-Burgos Laura, Wang Haiyun, Nieto Patricia, Zheng Jie, Blanco-Aparicio Carmen, Varela Carmen, Gómez-López Gonzalo, Fernández-García Fernando, Sanclemente Manuel, Guerra Carmen, Drosten Matthias, Galán Javier, Caleiras Eduardo, Martínez-Torrecuadrada Jorge, Fajas Lluis, Peng Sheng-Bin, Santamaría David, Musteanu Monica, Barbacid Mariano

Abstract excerpt

KRAS mutant lung adenocarcinomas remain intractable for targeted therapies. Genetic interrogation of KRAS downstream effectors, including the MAPK pathway and the interphase CDKs, identified CDK4 and RAF1 as the only targets whose genetic inactivation induces therapeutic responses without causing unacceptable toxicities. Concomitant CDK4 inactivation and RAF1 ablation prevented tumor progression and induced...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 32913049
DOI: 10.1073/pnas.2002520117
PMCID: PMC7533841

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